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Is glycation from exogenous ribose supplementation an issue?

glycation ribose nam nad niacinamide

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#1 zorba990

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Posted 23 September 2017 - 04:35 PM

Life extension published this article on ribose, which seems to refute the concern about glycation (over and above other carbs) please debate.

From : http://www.lifeexten...abolism/Page-02

Fibromyalgia (FM) and chronic fatigue syndrome are conditions that often occur together and are believed to have a similar underlying cause.28

There's accumulating evidence that defective production of ATP is the culprit.28-30 These findings make d-ribose a natural candidate as a therapy for those suffering from fibromyalgia and chronic fatigue syndrome. A published case study showed that a woman with fibromyalgia experienced a decrease in symptoms following supplementation with d-ribose.31 The patient had been unresponsive to prior medications, and her physicians based their decision on the known energy-enhancing capabilities of d-ribose.

A larger study soon followed enlisting 41 patients with fibromyalgia or chronic fatigue syndrome.28 Subjects took 5 grams of d-ribose three times daily until they reached a total of 280 grams.

There was significant improvement in all five categories on a standard score: energy, sleep, mental clarity, pain intensity, and well-being.28 On average, patients reported a 45% increase in energy levels.

While fibromyalgia and chronic fatigue syndrome remain complicated and perplexing to scientists, these findings offer real hope for a solution.

Restless Leg Syndrome
Restless Leg Syndrome
Restless leg syndrome (RLS) is a common disorder that affects as many as 15% of the US population, and it is severe enough to warrant medical treatment in more than a third of those people.32,33

The condition involves an uncontrollable urge to move the legs, accompanied by uncomfortable sensations, and it is usually worse at night.33 Only a few medications offer even partial relief of restless leg syndrome, and many make the condition worse—leaving sufferers without much recourse.32,33

Disordered energy metabolism has been suggested as one possible cause of restless leg syndrome. Low levels of adenosine, the d-ribose-containing central molecule in ATP, have been reported in those suffering from restless leg syndrome.34

Based on that observation, one study has been carried out in which daytime symptoms were eliminated, and nighttime symptoms significantly reduced, on daily doses of 15 grams of d-ribose, taken as one 5-gram dose with breakfast, lunch, and dinner.26

It's clearly too early to claim that d-ribose cures the condition, but these encouraging findings—coupled with complete absence of side effects—warrant further investigation.

It is now generally accepted that d-ribose supplementation provides many health benefits, particularly in the area of cellular energy management.

Several recent publications, however, have raised the question of whether d-ribose—because it is a sugar—could possibly contribute to development of harmful advanced glycation endproducts.40-43

The truth seems to be straightforward: Like any sugar, ribose can indeed cause protein glycation, with resulting damage to tissues.42 And when ribose is administered experimentally at the same high dose as glucose, ribose quickly causes the protein cross-linking that is the outcome of glycation.40

But those studies used artificially high doses and concentrations of ribose, levels never found in humans—even after high-dose supplementation.

For example, in a human study of d-ribose supplementation at doses of 20 and 53 grams over a 4-hour period, peak serum ribose levels rose to only 4.8 mg/dL and 81.7 mg/dL, respectively.44

But doses used in the glycation experiments were significantly higher, up to 30 times higher than achievable in human blood!42,43

And in an experiment showing that d-ribose induced glycation and impaired spatial cognition in mice, the ribose concentrations used were equivalent to blood levels of 150 to 750 mg/dL, clearly vastly higher than have been used in human studies.43,44

Researchers seeking to show that ribose-induced glycation could enhance cartilage damage in an animal model of osteoarthritis showed conclusively that even direct injection of ribose into the joint was incapable of triggering sufficient glycation to cause injury!45,46

The doses for d-ribose studies reported in this article—15 to 60 grams per day in divided doses—are incapable of causing serum ribose concentrations high enough to get anywhere near the risk of excessive glycation reported in the lab studies.44

Also, most human studies recommended splitting the total amount into three daily doses; this approach provides even greater assurance that serum d-ribose remains well within safe levels.

Kidney Protection
Like the brain and heart, the human kidney receives a a high proportion of the body's total blood flow—which makes it equally vulnerable to damage by ischemia-reperfusion mechanisms, the loss and restoration of blood flow.

These kidney injuries can occur as the result of trauma or during any major surgery, sometimes worsened by chronic conditions such as cardiovascular disease and diabetes.35-37

Growing evidence suggests that an immune activation and inflammatory response following this kind of kidney injury creates the bulk of the damage, especially in those with diabetes.12,38 Adenosine, which is partly made from d-ribose, is an important regulator of kidney function, and is especially vital during times of injury.39 These observations—coupled with what we know about d-ribose as antioxidant and anti-inflammatory—have aroused considerable interest among kidney researchers.

Japanese scientists have led the way in investigating d-ribose as a kidney protector. They have found that in rats subjected to renal ischemia-reperfusion—similar to what can occur during major surgery—d-ribose significantly reduced the release of inflammatory cytokines.12 Kidney function and appearance following the injury was improved substantially.

They also showed that d-ribose reduces activation of neutrophils, the ubiquitous white blood cells that are the first to arrive at the scene of an injury but that also release toxic chemicals and oxygen radicals that can cause additional harm.11

Clearly researchers are only beginning to realize the substantial potential of d-ribose for kidney health.

D-ribose is an essential component in our bodies' cellular energy management systems. Additionally, it provides antioxidant, anti-inflammatory, and gene regulatory capabilities. Together these characteristics make it of compelling interest to forward-thinking clinicians and patients.

Supplemental d-ribose demonstrates cardioprotection—even late in the disease process when heart attacks have already occurred, and when heart failure is developing. D-ribose helps ailing heart muscle maximize its effort, and improves blood flow to oxygen-starved cardiac tissue.

D-ribose supplements are only just being explored for similar benefits in brain and kidney tissues, but recent studies offer great hope in those areas. Even perplexing conditions such as fibromyalgia and restless leg syndrome seem to be yielding to the energy-related benefits of d-ribose. •

1. Miyoshi N, Oubrahim H, Chock PB, Stadtman ER. Age-dependent cell death and the role of ATP in hydrogen peroxide-induced apoptosis and necrosis. Proc Natl Acad Sci USA. 2006 Feb 7;103(6):1727-31. Epub 2006 Jan 27.

2. Kohlhaas M, Maack C. Interplay of defective excitation-contraction coupling, energy starvation, and oxidative stress in heart failure. Trends Cardiovasc Med. 2011 Apr;21(3):69-73.

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4. Barsotti C, Ipata PL. Pathways for alpha-D-ribose utilization for nucleobase salvage and 5-fluorouracil activation in rat brain. Biochem Pharmacol. 2002 Jan 15;63(2):117-22.

5. Omran H, McCarter D, St Cyr J, Luderitz B. D-ribose aids congestive heart failure patients. Exp Clin Cardiol. 2004 Summer;9(2):117-8.

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8. Freeman ML, Mertens-Talcott SU, St Cyr J, Percival SS. Ribose enhances retinoic acid-induced differentiation of HL-60 cells. Nutr Res. 2008 Nov;28(11):775-82.

9. Ferrari R, Pepi P, Ferrari F, Nesta F, Benigno M, Visioli O. Metabolic derangement in ischemic heart disease and its therapeutic control. Am J Cardiol. 1998 Sep 3;82(5A):2K-13K.

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11. Sato H, Ueki M, Asaga T, Chujo K, Maekawa N. D-ribose attenuates ischemia/reperfusion-induced renal injury by reducing neutrophil activation in rats. Tohoku J Exp Med. 2009 May;218(1):35-40.

12. Nishiyama J, Ueki M, Asaga T, Chujo K, Maekawa N. Protective action of D-ribose against renal injury caused by ischemia and reperfusion in rats with transient hyperglycemia. Tohoku J Exp Med. 2009 Nov;219(3):215-22.

13. Pauly DF, Pepine CJ. D-Ribose as a supplement for cardiac energy metabolism. J Cardiovasc Pharmacol Ther. 2000 Oct;5(4):249-58.

14. Pliml W, von Arnim T, Stablein A, Hofmann H, Zimmer HG, Erdmann E. Effects of ribose on exercise-induced ischaemia in stable coronary artery disease. Lancet. 1992 Aug 29;340(8818): 507-10.

15. Kendler BS. Supplemental conditionally essential nutrients in cardiovascular disease therapy. J Cardiovasc Nurs. 2006 Jan-Feb;21(1):9-16.

16. Sinatra ST. Metabolic cardiology: an integrative strategy in the treatment of congestive heart failure. Altern Ther Health Med. 2009 May-Jun;15(3):44-52.

17. Lopaschuk GD. Treating ischemic heart disease by pharmacologically improving cardiac energy metabolism. Presse Med. 1998 Dec 12;27(39):2100-4.

18. Pauly DF, Johnson C, St Cyr JA. The benefits of ribose in cardiovascular disease. Med Hypotheses. 2003 Feb;60(2):149-51.

19. Sinatra ST. Metabolic cardiology: the missing link in cardiovascular disease. Altern Ther Health Med. 2009 Mar-Apr;15(2):48-50.

20. Hegewald MG, Palac RT, Angello DA, Perlmutter NS, Wilson RA. Ribose infusion accelerates thallium redistribution with early imaging compared with late 24-hour imaging without ribose. J Am Coll Cardiol. 1991 Dec;18(7):1671-81.

21. Omran H, Illien S, MacCarter D, St Cyr J, Luderitz B. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study. Eur J Heart Fail. 2003 Oct;5(5):615-9.

22. Omran H, McCarter D, St Cyr J, Luderitz B. D-ribose aids congestive heart failure patients. Exp Clin Cardiol. 2004 Summer;9(2):117-8.

23. Schneider HJ, Rossner S, Pfeiffer D, Hagendorff A. D-ribose improves cardiac contractility and hemodynamics, and reduces expression of c-fos in the hippocampus during sustained slow ventricular tachycardia in rats. Int J Cardiol. 2008 Mar 28;125(1):49-56.

24. Sawada SG, Lewis S, Kovacs R, et al. Evaluation of the anti-ischemic effects of D-ribose during dobutamine stress echocardiography: a pilot study. Cardiovasc Ultrasound. 2009;7:5.

25. MacCarter D, Vijay N, Washam M, Shecterle L, Sierminski H, St Cyr JA. D-ribose aids advanced ischemic heart failure patients. Int J Cardiol. 2009 Sep 11;137(1):79-80.

26. Chigrinskiy EA, Conway VD. Protective effect of D-ribose against inhibition of rats testes function at excessive exercise. Journal of Stress Physiology & Biochemistr. 2011;7(3):242-9.

27. Barsotti C, Ipata PL. Pathways for alpha-D-ribose utilization for nucleobase salvage and 5-fluorouracil activation in rat brain. Biochem Pharmacol. 2002 Jan 15;63(2):117-22.

28. Teitelbaum JE, Johnson C, St Cyr J. The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study. J Altern Complement Med. 2006 Nov;12(9):857-62.

29. Eisinger J, Plantamura A, Ayavou T. Glycolysis abnormalities in fibromyalgia. J Am Coll Nutr. 1994 Apr;13(2):144-8.

30. Le Goff P. Is fibromyalgia a muscle disorder? Joint Bone Spine. 2006 May;73(3):239-42.

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32. Martin CM. The mysteries of restless legs syndrome. Consult Pharm. 2007 Nov;22(11):907-24.

33. Bayard M, Avonda T, Wadzinski J. Restless legs syndrome. Am Fam Physician. 2008 Jul 15;78(2):235-40.

34. Guieu R, Sampieri F, Pouget J, Guy B, Rochat H. Adenosine in painful legs and moving toes syndrome. Clin Neuropharmacol. 1994 Oct;17(5):460-9.

35. Laisalmi-Kokki M, Pesonen E, Kokki H, et al. Potentially detrimental effects of N-acetylcysteine on renal function in knee arthroplasty. Free Radic Res. 2009 Jul;43(7):691-6.

36. Siems W, Quast S, Carluccio F, et al. Oxidative stress in chronic renal failure as a cardiovascular risk factor. Clin Nephrol. 2002 Jul;58 Suppl 1:S12-9.

37. Yan SF, Ramasamy R, Schmidt AM. The receptor for advanced glycation endproducts (RAGE) and cardiovascular disease. Expert Rev Mol Med. 2009;11:e9.

38. Jang HR, Ko GJ, Wasowska BA, Rabb H. The interaction between ischemia-reperfusion and immune responses in the kidney. J Mol Med. 2009 Sep;87(9):859-64.

39. Vallon V, Osswald H. Adenosine receptors and the kidney. Handb Exp Pharmacol. 2009 (193):443-70.

40. Mentink CJ, Hendriks M, Levels AA, Wolffenbuttel BH. Glucose-mediated cross-linking of collagen in rat tendon and skin. Clin Chim Acta. 2002 Jul;321(1-2):69-76.

41. Kuo TY, Huang CL, Yang JM, et al. The role of ribosylated-BSA in regulating PC12 cell viability. Cell Biol Toxicol. 2012 Aug;28(4): 255-67.

42. Wei Y, Han CS, Zhou J, Liu Y, Chen L, He RQ. d-ribose in glycation and protein aggregation. Biochim Biophys Acta. 2012 Apr;1820(4):488-94.

43. Han C, Lu Y, Wei Y, Liu Y, He R. D-ribose induces cellular protein glycation and impairs mouse spatial cognition. PLoS One. 2011;6(9):e24623.

44. Gross M, Zollner N. Serum levels of glucose, insulin, and C-peptide during long-term D-ribose administration in man. Klin Wochenschr. 1991 Jan 4;69(1):31-6.

45. Vos PA, Degroot J, Barten-van Rijbroek AD, et al. Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage. J Orthop Res. 2012 Mar 2.

46. Willett TL, Kandel R, De Croos JN, Avery NC, Grynpas MD. Enhanced levels of non-enzymatic glycation and pentosidine crosslinking in spontaneous osteoarthritis progression. Osteoarthritis Cartilage. 2012 Jul;20(7):736-44."

Edited by zorba990, 23 September 2017 - 04:38 PM.

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